by You probably referred to them negatively – blaming them for your weight, bad habits or thinning hair. But while you can’t change the genetic hand you’ve been dealt, you have more control over how your genes work than you think.
We are born with around 20,000 genes, which are stretches of DNA that contain instructions for our cells. There are two copies of each – one inherited from each of our parents.
Scientists know that some genes carry a higher risk of ill health. For example, certain genetic variants can increase your risk of obesity, Alzheimer’s and cancer.
However, lifestyle habits are intertwined with how our genes are expressed and can effectively turn certain ones “on” or “off” – like light switches in your home.
Ultimately, this means that, in many cases, you can turn down genes linked to disease and dial up those associated with longevity.
“Studies have shown that longevity in humans is about 25 percent heritable. What it means is that the environment largely (75 percent) determines how long we live and our genes only have 25 percent,” says Professor Joao Pedro Magalhaes, head of the Aging and Regeneration Genomics Laboratory at the National University of Ireland. Birmingham.
“If you exercise, that triggers changes in your body that affect how your genes are expressed. The same goes for diet.”
It is “very difficult” to draw a line between lifestyle changes, a change in gene expression and the effect on longevity, according to Professor Magalhaes. However, some research is promising.
Calorie restriction
“There is a gene called mTOR that controls how our cells perceive nutrients and – depending on that – decides whether to grow or not,” explains Dr Nick Ktistakis, group leader at the Babraham Institute, where researchers studying the aging process.
“Decreasing mTOR activity has been shown to extend lifespan in many organisms, and would likely do so in humans. Therefore, reducing mTOR activity is good for longevity,” he says.
One way to effectively turn off mTOR is to cut back on calories, according to animal studies, whose food intake was cut in half.
However, scientists admit that this is not possible due to the “strong force power” that would be required in humans to do so and they clearly warn that the approach could have dangerous side effects. motivation, such as losing too much weight.
Therefore, researchers are studying another pharmaceutical option – a drug called rapamycin. It was originally developed as an immunosuppressant for organ transplant patients but, like calorie restriction, it suppresses mTOR. “A lot of work is being done with these drugs to see if they can affect longevity,” says Dr. Ktistakis.
“Rapamycin is one of the most potent lifespan-extending drugs because it extends the lifespan of rodents (up to 15 percent) and is currently being tested in dogs. [It] is one of the most active research areas in longevity pharmacology,” says Professor Magalhaes.
However, separate studies have supported the evidence for calorie cutting to live longer. A team at Columbia University found that people who cut their food intake by 25 percent for two years slowed their biological aging by two to three percent. That conclusion was reached after they took blood samples from the volunteers to monitor chemical tags that regulate the expression of genes associated with longevity.
The researchers noted that while dramatic calorie cutting is probably not “for everyone”, simply following intermittent fasting (eating little or nothing for a set period of time, such as one or two days a week) or eating time constraints. (eating within a fixed window each day, such as 10am and 6pm, may produce similar results).
Exercise
Scientists are also excited about a gene called FOXO3. Studies going back more than a decade show that it activates autophagy – the process by which cells get rid of old and damaged parts, which is crucial to increasing a healthy lifespan.
Although everyone has two copies of it, as with all genes, three in 10 people in the UK have one “supercharged” version, and one in 10 have two – meaning the FOXO3 “jet” gene of them, according to Dr Craig. Willcox, professor of public health and gerontology at Okinawa International University in Japan. Only a genetic test can show which version a person has.
“Our studies have shown that FOXO3 is at the heart of the aging hub. It integrates signals from dozens of other genes that affect the aging process. Think of it as a caretaker gene that directs the aging process as well as protection against age-related diseases,” he says.
Research has shown that FOXO3 protects against cardiovascular disease – one of the leading causes of death in the UK – and cardiometabolic disease, including heart attack, diabetes and non-alcoholic fatty liver disease.
Exercise can turn on FOXO3 by telling it “it needs to go to work” and counterbalance the stress that physical activity puts on the body, explains Dr Willcox. In response, FOXO3 stimulates the release of antioxidants that reduce inflammation.
How quickly the gene is activated depends on the person’s genes and lifestyle. But it’s likely to happen slowly over time, “just like working out will change your body shape over time”, he says. “The key to making a lifestyle change is persistence and continuity,” says Dr Willcox.
Sleep
Other studies show that sleep is vital.
When scientists at the University of Rochester compared how genes were regulated across many animals, they found that among the longest-lived species, genes associated with inflammation and the process of converting food into energy were reduced.
Rather than the expression of these genes being predetermined, whether to dial them up or down is controlled by the body’s circadian network – also known as the body’s internal clock.
The team concluded that this meant that an unhealthy sleep schedule or exposure to light at night could increase the expression of genes that describe lifespan in humans, despite their studies focusing on animals.
Drink green tea and eat broccoli, oranges and berries
“AMPK is often seen as the ‘master switch’ of our metabolism and is also seen as a central junction for many nutrient-responsive pathways associated with longevity,” says Dr. Harpal Bains, medical director of the Harpal Clinic focused on longevity in London.
Both green tea and the antioxidant quercetin—found in onions, broccoli, citrus fruits and berries—can activate AMPK, she says.
“Finding good quality green tea is a good foundational way to support longevity as green tea can support many areas of genetic expression,” says Dr Bains.
Calorie restriction and exercise also dial up this gene, she says.
“Caloric restriction is definitely not about eating as little as possible,” notes Dr. Harpal. “This would be unhealthy, it would cause nutritional deficiencies and as a result we would not have enough fuel – it would not be very good for our longevity at all. Instead it’s more about not overeating: we should aim to feel about 80 per cent full with each meal.”
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